Glocoma reason, treatment and complications
glaucoma treatment management

| Drug Class | Examples | Mechanism |
|---|---|---|
| Prostaglandin analogues (first choice) | Latanoprost, bimatoprost, travoprost, tafluprost | Increase aqueous outflow; once-daily dosing, low side effects |
| Beta-blockers | Timolol, betaxolol, levobunolol | Decrease aqueous secretion from ciliary epithelium |
| Alpha-2 agonists | Brimonidine, apraclonidine | Decrease aqueous secretion + increase outflow |
| Carbonic anhydrase inhibitors | Dorzolamide (topical), acetazolamide (oral) | Decrease aqueous secretion |
| Rho-kinase inhibitors | Netarsudil | Increase outflow (newer agent) |
| Cholinomimetics | Pilocarpine, carbachol | Ciliary muscle contraction opens trabecular meshwork |
Prostaglandin analogues are currently the drugs of choice to initiate treatment - effective, once-daily dosing, and low adverse effect profile. Beta-blockers should be used with caution in patients with bradycardia, heart block, heart failure, or asthma.
| Complication | Details |
|---|---|
| Blindness (irreversible) | The end-stage of untreated or uncontrolled glaucoma; second leading cause of blindness worldwide |
| Visual field loss | Starts peripherally, progresses centrally; often unnoticed until severe |
| Optic nerve atrophy | Diffuse loss of ganglion cells and thinning of the retinal nerve fiber layer; optic disc becomes cupped and atrophic |
| Corneal edema/bullous keratopathy | Acute IOP spikes (especially in angle-closure) can cause corneal endothelial damage |
| Cataract | Secondary to chronic elevated IOP, medications, or surgical intervention |
| Buphthalmos | Globe enlargement from chronically elevated IOP in infants (congenital glaucoma) |
| Treatment complications | Trabeculectomy can cause choroidal effusion, suprachoroidal hemorrhage, or wound leak; tube shunts can erode through conjunctiva; topical beta-blockers can cause systemic bradycardia/bronchospasm |
| Amblyopia | In children with congenital glaucoma if untreated early |